Studies on platelet function of newborn term infants have demonstrated impaired aggregation in response to collagen and epinephrine. Further investigations in prematurely born infants and in primate fetuses have indicated progressive impairment of platelet function with decreasing gestational age. Measurement of the components of cyclic AMP metabolism, including adenyl cyclase and phosphodiesterase will be made on the platelets of full-term and premature newborn infants in an attempt to identify the bio-chemical basis for the functional abnormalities. Employing cultures of skin fibroblasts the development of tissue factor activity in the human fetus and newborn will be investigated. Evidence has been presented by others to suggest that a plasmo co- factor needed for ristocetin-induced platelet aggregation may be the Von Willebrand factors. Studies of the development of this factor in the plasma of fetuses and newborns will be undertaken. Using "platelet-injury" and immunologic techniques, a systematic study of the incidence and prognostic significance of anti-platelet antibodies in idiopathic thrombo cytopenic purpura in children will be undertaken. Severe and recurring epistaxis in childhood remains unexplained in most instances. In order to determine whether the platelet of such children are abnormally susceptible to inhibition, dose-response inhibition of aggregation will be studied using PGE1, theophylline, and aspirin as the inhibiting agents and collagen, epinephrine and thrombin as the aggregating agents.